CAJ | 학술논문

目的探讨在肝损伤早期酒精和HBV协同作用的分子机制.方法 20只HBV转基因小鼠和20只普通小鼠随机分为4组:转基因小鼠酒精组(alcohol-fed Tg mice)和普通小鼠酒精组(alcohol-fed Wt mice),以白酒灌胃;转基因小鼠对照组(control Tg mice)和普通小鼠对照组(control Wt mice),以生理盐水灌胃.连续处理10 wk后检测各组小鼠血清ALT、AST水平,肝组织转化生长因子-β_1(TGF-β_1)、Smad3、Smad7、结缔组织生长因子 (CTGF) mRNA表达水平及TGF-β_1、CTGF、α-平滑肌肌动蛋白(α-SMA)蛋白表达水平.结果酒精可升高转基因小鼠血清ALT、AST水平,诱发其肝脏病理损伤,但纤维化不明显;肝组织TGF-β_1、Smad3、Smad7、CTGF mRNA及TGF-β_1、CTGF、α-SMA蛋白表达增加.结论酒精和HBV对肝损伤协同作用的机制可能与TGF-β_1、Smad3、CTGF、α-SMA表达增加以及TGF-β_1/Smads通路信号分子表达比例失调有关.
목적 탐토재간손상조기주정화HBV협동작용적분자궤제.방법 20지HBV전기인소서화20지보통소서수궤분위4조:전기인소서주정조(alcohol-fed Tg mice)화보통소서주정조(alcohol-fed Wt mice),이백주관위;전기인소서대조조(control Tg mice)화보통소서대조조(control Wt mice),이생리염수관위.련속처리10 wk후검측각조소서혈청ALT、AST수평,간조직전화생장인자-β_1(TGF-β_1)、Smad3、Smad7、결체조직생장인자 (CTGF) mRNA표체수평급TGF-β_1、CTGF、α-평활기기동단백(α-SMA)단백표체수평.결과 주정가승고전기인소서혈청ALT、AST수평,유발기간장병리손상,단섬유화불명현;간조직TGF-β_1、Smad3、Smad7、CTGF mRNA급TGF-β_1、CTGF、α-SMA단백표체증가.결론 주정화HBV대간손상협동작용적궤제가능여TGF-β_1、Smad3、CTGF、α-SMA표체증가이급TGF-β_1/Smads통로신호분자표체비례실조유관.
Aim To investigate the synergistic effects and possible molecular mechanism of hepatitis B virus (HBV) and alcohol on liver injury in HBV transgenic mice(HBV-Tg mice).Methods 20 HBV-Tg mice and 20 wild-type mice were randomly divided into 4 groups:alcohol-fed Tg mice and alcohol-fed Wt mice, and they were given intragastric administration with alcohol. Control Tg mice and control Wt mice received intragastric administration with saline.All groups were rasied for 10 weeks.The levels of ALT and AST in serum, the degree of inflammation, the degree of fibrosis, the mRNA expression of TGF-β_1, Smad3, Smad7, CTGF and the protein expression of TGF-β_1, CTGF, α-SMA in liver tissue were detected.Results The serumlevel of ALT and AST, the mRNA expression of TGF-β_1, Smad3, Smad7, CTGF and the protein expression of TGF-β_1, CTGF, α-SMA in liver all increased markedly in alcohol-fed Tg mice. Alcohol consumption induced hepatocyte steatosis and hepatic inflammation in alcohol-fed Tg mice, but the change of liver fibrosis was not remarkable.Conclusion HBV and alcohol have synergistic effects on early liver injury, possibly by enhancing the expression of TGF-β_1, Smad3, CTGF, α-SMA and inducing unbalanced expression of Smads.